Results 261 to 270 of about 74,541 (281)

Edible and Medicinal Fritillaria thunbergii Miq. Aqueous Extract Improves Metabolic Health via Modulation of Gut Microbiota in Mice Fed on a High‐Sugar and High‐Fat Diet

open access: yesJournal of Food Biochemistry, Volume 2026, Issue 1, 2026.
Fritillaria thunbergii Miq. (FTM), a traditional medicinal and edible herb, has shown promise in alleviating metabolic disturbances, yet its mechanistic basis remains unclear. In this study, we investigated the therapeutic effects of FTM aqueous extract in a male KM mouse model of obesity induced by a high‐sugar, high‐fat diet (HSFD).
Linen Zou   +10 more
wiley   +1 more source

Renalase deficiency suppresses hepatic triglyceride accumulation in the progression to MASLD/MASH by GAN diet in male mice

open access: yesPhysiological Reports, Volume 14, Issue 2, January 2026.
Abstract Metabolic dysfunction‐associated steatotic liver disease (MASLD) is a growing public health concern characterized by hepatic triglyceride (TG) accumulation, inflammation, and fibrosis. Renalase is known for its role in blood pressure regulation and catecholamine metabolism, but recent evidence suggests broader cytokine‐like functions. Moreover,
Yota Okano   +5 more
wiley   +1 more source

Inducible Ift88‐deficient mice show features consistent with mild pulmonary hypertension

open access: yesPhysiological Reports, Volume 14, Issue 2, January 2026.
Abstract Intraflagellar transport protein 88 (IFT88) is essential for primary and motile cilia formation. In murine models and humans, Ift88 mutations contribute to renal cysts, epithelial proliferation and impaired immune responses. In mice, Ift88 knockout (KO) reduces airway cilia, increases airway epithelial proliferation and hyperreactivity ...
Selina M. Garcia   +10 more
wiley   +1 more source

Understanding Keratoconus in Down Syndrome: From Etiology to Management - A Narrative Review. [PDF]

open access: yesClin Ophthalmol
Anitha V   +7 more
europepmc   +1 more source

Distinct amyloid fibril structures formed by ALS-causing SOD1 mutants G93A and D101N. [PDF]

open access: yesEMBO Rep
Zhang MY   +11 more
europepmc   +1 more source

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